Metabolic consequences of obesity on the hypercoagulable state of polycystic ovary syndrome

Abstract Polycystic ovary syndrome (PCOS) women have a hypercoagulable state; however, whether this is intrinsically due to PCOS or, alternatively, a consequence of its metabolic complications is unclear. We determined plasma coagulation pathway protein levels in PCOS (n = 146) and control (n = 97)...

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Autores principales: Abu Saleh Md Moin, Thozhukat Sathyapalan, Ilhame Diboun, Mohamed A. Elrayess, Alexandra E. Butler, Stephen L. Atkin
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Publicado: Nature Portfolio 2021
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spelling oai:doaj.org-article:e51be4a72d3e48818948f31b3f80c4ae2021-12-02T13:34:46ZMetabolic consequences of obesity on the hypercoagulable state of polycystic ovary syndrome10.1038/s41598-021-84586-y2045-2322https://doaj.org/article/e51be4a72d3e48818948f31b3f80c4ae2021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-84586-yhttps://doaj.org/toc/2045-2322Abstract Polycystic ovary syndrome (PCOS) women have a hypercoagulable state; however, whether this is intrinsically due to PCOS or, alternatively, a consequence of its metabolic complications is unclear. We determined plasma coagulation pathway protein levels in PCOS (n = 146) and control (n = 97) women recruited to a PCOS biobank. Circulating levels of a panel of 18 clotting pathway proteins were determined by Slow Off-rate Modified Aptamer-scan plasma protein measurement. Cohorts were age matched, though PCOS had elevated body mass index (p < 0.001), insulin (p < 0.001) and C-reactive protein (CRP) (p < 0.0001). Eight pro-coagulation proteins were elevated in PCOS: plasminogen activator inhibitor-1 (p < 0.0001), fibrinogen (p < 0.01), fibrinogen gamma chain (p < 0.0001), fibronectin (p < 0.01), von Willebrand factor (p < 0.05), D-dimer (p < 0.0001), P-selectin (p < 0.05), and plasma kallikrein (p < 0.001). However, two anticoagulant proteins, vitamin K-dependent protein-S (p < 0.0001) and heparin cofactor-II (p < 0.001) were elevated and prothrombin was decreased (p < 0.05). CRP, as a marker of inflammation, and insulin resistance (HOMA-IR) correlated with 11 and 6 of the clotting proteins, respectively (p < 0.05). When matched for BMI < 25 (16 PCOS, 53 controls) HOMA-IR remained elevated (p < 0.05) and heparin cofactor-II was increased (p < 0.05). In a multivariate analysis accounting for inflammation, insulin resistance and BMI, there was no correlation of PCOS with any of the coagulation proteins. The hypercoagulable state in PCOS is not intrinsic to the disease as it can be fully accounted for by BMI, inflammation and insulin resistance.Abu Saleh Md MoinThozhukat SathyapalanIlhame DibounMohamed A. ElrayessAlexandra E. ButlerStephen L. AtkinNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-7 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Abu Saleh Md Moin
Thozhukat Sathyapalan
Ilhame Diboun
Mohamed A. Elrayess
Alexandra E. Butler
Stephen L. Atkin
Metabolic consequences of obesity on the hypercoagulable state of polycystic ovary syndrome
description Abstract Polycystic ovary syndrome (PCOS) women have a hypercoagulable state; however, whether this is intrinsically due to PCOS or, alternatively, a consequence of its metabolic complications is unclear. We determined plasma coagulation pathway protein levels in PCOS (n = 146) and control (n = 97) women recruited to a PCOS biobank. Circulating levels of a panel of 18 clotting pathway proteins were determined by Slow Off-rate Modified Aptamer-scan plasma protein measurement. Cohorts were age matched, though PCOS had elevated body mass index (p < 0.001), insulin (p < 0.001) and C-reactive protein (CRP) (p < 0.0001). Eight pro-coagulation proteins were elevated in PCOS: plasminogen activator inhibitor-1 (p < 0.0001), fibrinogen (p < 0.01), fibrinogen gamma chain (p < 0.0001), fibronectin (p < 0.01), von Willebrand factor (p < 0.05), D-dimer (p < 0.0001), P-selectin (p < 0.05), and plasma kallikrein (p < 0.001). However, two anticoagulant proteins, vitamin K-dependent protein-S (p < 0.0001) and heparin cofactor-II (p < 0.001) were elevated and prothrombin was decreased (p < 0.05). CRP, as a marker of inflammation, and insulin resistance (HOMA-IR) correlated with 11 and 6 of the clotting proteins, respectively (p < 0.05). When matched for BMI < 25 (16 PCOS, 53 controls) HOMA-IR remained elevated (p < 0.05) and heparin cofactor-II was increased (p < 0.05). In a multivariate analysis accounting for inflammation, insulin resistance and BMI, there was no correlation of PCOS with any of the coagulation proteins. The hypercoagulable state in PCOS is not intrinsic to the disease as it can be fully accounted for by BMI, inflammation and insulin resistance.
format article
author Abu Saleh Md Moin
Thozhukat Sathyapalan
Ilhame Diboun
Mohamed A. Elrayess
Alexandra E. Butler
Stephen L. Atkin
author_facet Abu Saleh Md Moin
Thozhukat Sathyapalan
Ilhame Diboun
Mohamed A. Elrayess
Alexandra E. Butler
Stephen L. Atkin
author_sort Abu Saleh Md Moin
title Metabolic consequences of obesity on the hypercoagulable state of polycystic ovary syndrome
title_short Metabolic consequences of obesity on the hypercoagulable state of polycystic ovary syndrome
title_full Metabolic consequences of obesity on the hypercoagulable state of polycystic ovary syndrome
title_fullStr Metabolic consequences of obesity on the hypercoagulable state of polycystic ovary syndrome
title_full_unstemmed Metabolic consequences of obesity on the hypercoagulable state of polycystic ovary syndrome
title_sort metabolic consequences of obesity on the hypercoagulable state of polycystic ovary syndrome
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/e51be4a72d3e48818948f31b3f80c4ae
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